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(Circulation. 2004;109:2263-2265.)
© 2004 American Heart Association, Inc.

Brief Rapid Communications

Clinical Recovery From End-Stage Heart Failure Using Left-Ventricular Assist Device and Pharmacological Therapy Correlates With Increased Sarcoplasmic Reticulum Calcium Content but Not With Regression of Cellular Hypertrophy

C.M.N. Terracciano, MD, PhD; J. Hardy, MBBS, BSc; E.J. Birks, MRCP, PhD; A. Khaghani, FRCS; N.R. Banner, FRCP; M.H. Yacoub, FRS

From Imperial College London, National Heart and Lung Institute, Harefield Heart Science Centre, Harefield, UK.

Correspondence to Dr Cesare M.N. Terracciano, Cellular Electrophysiology, Imperial College London, NHLI, Harefield Heart Science Centre, Harefield Hospital, Harefield, Middlesex UB9 6JH, UK. E-mail c.terracciano{at}imperial.ac.uk

Received January 13, 2004; de novo received February 25, 2004; revision received March 30, 2004; accepted March 31, 2004.

Background— Left ventricular assist device (LVAD) treatment is known to lead to structural and functional cellular modifications in the heart. The relevance of these changes for clinical recovery is unknown.

Methods and Results— We compared properties of cardiomyocytes obtained from tissue taken at explantation of the LVAD in patients with clinical recovery with those obtained from hearts of patients who did not show clinical recovery, thus requiring transplantation. Compared with myocytes taken at implantation, both the recovery and nonrecovery groups showed 50% reduction in cell capacitance, an index of cell size. However, action potential duration shortened, L-type Ca²⁺ current fast inactivation was more rapid, and sarcoplasmic reticulum Ca²⁺ content was increased in the recovery compared with the nonrecovery group.

Conclusions— These results show that specific changes in excitation-contraction coupling, and not regression of cellular hypertrophy, are specifically associated with clinical recovery after LVAD and further identify sarcoplasmic reticulum Ca²⁺ handling as a key functional determinant in patients with heart failure.

Key Words: mechanical devices • electrophysiology • heart failure • myocytes • sarcoplasmic reticulum

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